Type I interferons (IFNs) facilitate cancer immunosurveillance, antitumor immunity and antitumor efficacy of conventional cell death-inducing therapies (chemotherapy/radiotherapy) as well as immunotherapy. Moreover, it is clear that dendritic cells (DCs) play a significant role in aiding type I IFN-driven immunity. Owing to these antitumor properties several immunotherapies involving, or inducing, type I IFNs have received considerable clinical attention, e.g., recombinant IFNα2 or agonists targeting pattern recognition receptor (PRR) pathways like Toll-like receptors (TLRs), cGAS-STING or RIG-I/MDA5/MAVS. A series of preclinical and clinical evidence concurs that the success of anticancer therapy hinges on responsiveness of both cancer cells and DCs to type I IFNs. In this article, we discuss this link between type I IFNs and DCs in the context of cancer biology, with particular attention to mechanisms behind type I IFN production, their impact on DC driven anticancer immunity, and the implications of this for cancer immunotherapy, including DC-based vaccines.
Keywords: Apoptosis; Danger signals; IFNAR; Immune checkpoint blockers; Immunogenic cell death; Interferon stimulated genes; JAK-STAT pathway; Oncolytic viruses; Tumor immunology; Tumor microenvironment.
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